Redox homeostasis has been implicated in
subarachnoid hemorrhage (SAH). As a result,
antioxidants and/or
free radical scavengers have become an important therapeutic modality. Considering that
radix trichosanthis (RT)
saponins exhibited strong
antioxidant ability both in vivo and in vitro, the present study aimed to reveal whether the neuroprotective activities of RT
saponins were mediated by p38/p53 signal pathway after SAH. An established SAH model was used and
superoxide dismutase (SOD),
malondialdehyde (MDA), induced
nitric oxide synthase (iNOS),
nitric oxide (NO),
lactate dehydrogenase (LDH), p-p38, and p53 activation were detected after 48 h of SAH. The results showed that RT
saponins inhibited iNOS expression to restore NO to basal level. Moreover, compared with Cu/Zn-SOD, RT
saponins (2 mg/kg/d dosage) significantly increased
Mn-SOD activity after SAH. Accompanied with lowered NO and elevated SOD, decreased p38 phosphorylation and p53 activities were observed, especially for RT
saponins at 2 mg/kg/d dosage. In this setting, the neurological outcome was also improved with less neuronal cells damage after RT
saponins pretreatment. Our findings demonstrated the beneficial effects of RT
saponins in enhancing
neuroprotective effects by deducing iNOS activity, normalizing SOD level, and inhibiting p-p38 and p53 expression, hence offering significant therapeutic implications for SAH.